By Carolina Lima | Published on February 13, 2026 | 3 min read
Hypertrophic
cardiomyopathy (HCM) remains a major concern
in sports cardiology because it is among the leading causes of sudden
cardiac death (SCD) in young competitive athletes. In a large US registry
of 1,866 athlete deaths, HCM accounted for nearly 40% of cases, most
occurring in adolescents still in high school. More than 80% of these
individuals were asymptomatic prior to collapse, underscoring how difficult it
is to identify HCM before catastrophic events occur.
Physiological
vs Pathological
A consistent challenge in
evaluating young athletes is distinguishing physiological left‑ventricular
hypertrophy (LVH), the result of intensive training, from the pathological
hypertrophy characteristic of HCM.
Endurance training
remodels the heart through increased LV wall thickness, cavity enlargement and
enhanced diastolic filling. Up to 20% of young athletes develop LVH,
though most remain below the 12 mm threshold considered normal
for athletic adaptation. However, a subset—particularly male endurance
athletes and African American athletes—may develop wall thickness between
13–16 mm. This “grey zone” provides limited diagnostic clarity.
Unlike LVH, HCM is
marked by asymmetric septal hypertrophy (≥15 mm), a small LV cavity,
impaired relaxation and potentially left ventricule outflow tract
obstruction (LVOTO), a narrowing of the outflow tract during systole
increasing the pressure gradient between the LV and the aorta. LVOTO
contributes to symptoms such as exertional chest pain, dyspnea, dizziness and
syncope and may be present in one‑third of patients at rest and in up to
70% during exercise. Importantly, such obstructive physiology is not
observed in athletes with purely LVH.
ECG and imaging clues
Electrocardiography is
one of the most helpful first‑line diagnostic tools. T‑wave inversion (TWI) is the most
common ECG hallmark of HCM, appearing in over 75% of
athletes with the condition. Importantly, healthy athletes do not show
pathological TWI, ST depression or Q waves.
Echocardiography also plays a
central role. Physiological LVH is typically symmetric,
accompanied by a significantly enlarged LV cavity (55–70 mm),
whereas HCM usually presents with smaller cavity dimensions (<50
mm). An LV cavity size >54
mm has been shown
to effectively distinguish athlete’s heart from HCM, though a small minority of
athletes with HCM may still exceed this value.
Cardiac MRI (CMR) provides an
additional tips for diagnostic and is the gold
standard for structural assessment, particularly with its ability to detect
fibrosis and measure extracellular volume (ECV). Elevated ECV
and T1 values suggest pathological hypertrophy. An ECV threshold
>22.5% offers excellent sensitivity and specificity for distinguishing
HCM from athletic remodeling.
Exercise physiology
Functional assessment
further highlights the contrast between physiological and pathological
remodeling.
Athletes with LVH typically achieve high peak oxygen consumption (VO₂max
>50 ml/kg/min). In contrast, individuals with HCM often fail
to augment stroke volume appropriately during exercise. Exercise testing may
reveal abnormal blood-pressure responses, ST‑segment changes or ventricular
arrhythmias in HCM.
These exercise‑induced limitations help explain why some individuals with
HCM, despite appearing structurally similar to athletes, cannot perform
athletically at an elite level.
Detraining
studies provide additional insight: LVH regresses with weeks of reduced
activity, whereas HCM-related abnormalities persist, offering a practical
diagnostic strategy when uncertainty remains.
Implications for sports eligibility
Given
the unpredictable risk of arrhythmogenic events in HCM, both American and
European guidelines traditionally advise against participation in moderate and
high‑intensity sports for phenotype‑positive individuals. Genotype‑positive but
phenotype‑negative athletes remain more controversial: European guidelines
adopt a more conservative posture, while US recommendations permit full
participation with structured follow‑up.
A structured
evaluation—integrating ECG, echocardiography, CMR, and exercise
physiology—remains essential to prevent misdiagnosis and reduce the risk of
sudden cardiac death in young athletes.
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À propos de l’auteure – Carolina LimaDocteure spécialisée en anesthésiologie
Carolina est spécialiste en anesthésiologie et nourrit une profonde passion pour l’apprentissage et le partage des connaissances médicales. Dévouée à l’avancement de sa discipline, la Dre Lima s’efforce d’apporter à la communauté médicale des perspectives nouvelles fondées sur les données probantes. Considérant la médecine non pas simplement comme une profession, mais comme un parcours d’apprentissage continu tout au long de la vie, la Dre Lima s’engage à rendre l’information complexe claire, pratique et utile pour les professionnels de santé du monde entier.
